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Oral KCl Supplementation Safely Reduces Body Na+ Surplus and Blood Pressure
PMU Author
Adriana Marton
All Authors
Adriana Marton, Hieu T N Tran, Norihiko Morisawa, Ismail Osman, Seyed Ehsan Saffari, Tzy Tiing Lim, Wan Keat Yam, Matthew B Chuah, Wei Lin Tay, Wai Lun Moy, Pek-Lan Khong, Calvin W L Chin, Armin M Nagel, Roger S Y Foo, Friedrich C Luft, Eric Finkelstein, Jean-Paul Kovalik, Manfred Rauh, Troy Puar, Jens Titze
Journal association
CIRCULATION RESEARCH
Abstract
BACKGROUND: Potassium-enriched table salt lowers blood pressure (BP) and reduces cardiovascular mortality. Whether these beneficial effects stem from reduced Na+ intake, increased K+ intake, or both is unknown. We tested the hypothesis that oral potassium chloride (KCl) supplementation lowers body Na+ content and BP in patients with essential hypertension (EH) or hyperaldosteronism, independent of salt intake.
METHODS: Between February 2024 and February 2025, we conducted a single-arm, prospective, longitudinal study with nonrandomized oral KCl intervention in 40 participants with hypertension. All received personalized (blood K+-adjusted) KCl supplementation (Span-K tablets) for 6 to 9 weeks. After the intervention, participants completed a routine diagnostic workup and were classified with EH or hyperaldosteronism. Primary end point: baseline muscle Na+ surplus in hyperaldosteronism. Secondary end point: interventional muscle Na+ mobilization and BP reduction.
RESULTS: Seventeen participants were diagnosed with EH, and 23 with hyperaldosteronism. At baseline, patients with hyperaldosteronism showed higher muscle Na+ content (24.67±2.93 versus 22.48±3.37 mmol/L tissue volume, P=0.023; primary end point). Oral KCl increased 24-hour urine K+ excretion without altering 24-hour urine Na+. KCl supplementation successfully eliminated the muscle Na+ surplus in the hyperaldosteronism group (-1.90 mmol/L tissue volume [CI, -3.20 to -0.60]; P=0.005; secondary end point), lowered blood Na+/K+ ratios in both groups (EH, -5.34 [CI, -7.69 to -2.99]; P=4.6×10-5; hyperaldosteronism, -7.02 [CI, -9.04 to -5.01]; P=2.1×10-8), and reduced systolic BP (EH, -8.33 mm Hg [CI, -14.55 to -2.12]; P=0.010; hyperaldosteronism, -7.35 mm Hg [CI, -12.69 to -2.01]; P=0.008). To account for early study termination, a conservative significance threshold of α=0.025 was implemented, which all end points crossed.
CONCLUSIONS: Oral KCl supplementation mobilizes intracellular Na+ stores, corrects pathological Na+/K+ distribution, and lowers BP across hypertension phenotypes. This safe, targeted approach warrants consideration as a scalable public health strategy for cardiovascular disease prevention.
REGISTRATION: URL: www.clinicaltrials.gov; Unique identifier: NCT06569589.